Intravenous Lipid Administration Research Articles

Lipid emulsion therapy during management of the critically-ill poisoned patient: a prospective cohort study

Background Despite conflicting data, intravenous lipid emulsion has emerged as a potential antidote. The “lipid sink” theory suggests that following intravenous administration of lipid, lipophilic drugs are sequestered in the vascular compartment, thereby reducing their tissue concentrations. This study sought to determine if survival is associated with the intoxicant’s degree of lipophilicity. Methods We reviewed all cases in the Toxicology Investigators Consortium’s lipid sub-registry between May 2012 through December 2018. Information collected included demographics, exposure circumstances, clinical course, management, disposition, and outcome. The primary outcome was survival after lipid emulsion therapy. Survival was stratified by the log of the intoxicant’s octanol-water partition coefficient. We also assessed the association between intoxicant lipophilicity and an increase in systolic blood pressure after lipid emulsion administration. Results We identified 134 patients, including 81 (60.4%) females. The median age was 40 years (interquartile range 21-75). One hundred and eight (80.6%) patients survived, including 45 (33.6%) with cardiac arrest during their intoxication. Eighty-two (61.2%) were hypotensive, and 98 (73.1%) received mechanical ventilation. There was no relationship between survival and the log of the partition coefficient of the intoxicant on linear analysis (P = 0.89) or polynomial model (P = 0.10). Systolic blood pressure increased in both groups. The median (interquartile range) systolic blood pressure before lipid administration was 68 (60-78) mmHg for those intoxicants with a log partition coefficient < 3.6 compared with 89 (76-104) mmHg after lipid administration. Among those drugs with a log partition coefficient > 3.6, the median (interquartile range) was 69 (60-84) mmHg before lipid and 89 (80-96) mmHg after lipid administration. Conclusion Most patients in this cohort survived. Lipophilicity was not correlated with survival or the observed changes in blood pressure. The study did not address the efficacy of lipid emulsion.

Systemic Exposure, Metabolism, and Elimination of [14C]-Labeled Amino Lipid, Lipid 5,After a Single Administration of mRNA Encapsulating Lipid Nanoparticles to Sprague Dawley Rats.

The emerging therapeutic modality of lipid nanoparticle (LNP)-encapsulated mRNAs has demonstrated promising clinical results when used as vaccines and is currently being tested in formulations for a wide range of targeted chronic disease treatments. These therapeutics are multicomponent assemblages of well-characterized naturally occurring molecules in addition to xenobiotic molecules, whose in vivo distributions are poorly understood. Here, the metabolic outcome and in vivo elimination of Lipid 5, a key xenobiotic amino lipid in LNP formulations, were assessed after intravenous administration of 14C-labeled Lipid 5 to Sprague Dawley rats. Intact Lipid 5 was predominantly cleared from plasma within 10 h after dosing, with only small quantities (<1% of 14C dose) of a single diacid metabolite detected after 10 h. Lipid 5 was rapidly metabolized via ester hydrolysis into aliphatic alcohols and diacidic amino head group moieties, which were further metabolized via β-oxidation. Overall, >90% of the administered Lipid 5-derived 14C was recovered in urine (65%) and feces (35%), predominantly as oxidative metabolites, within 72 h after dosing, indicating rapid renal and hepatic elimination. In vitro metabolite identification after incubation with human, nonhuman primate, and rat hepatocytes showed similar metabolites to those found in vivo. No meaningful differences were observed in Lipid 5 metabolism or elimination by sex. In conclusion, Lipid 5, a critical amino lipid component of LNPs for mRNA therapeutic delivery, showed minimal exposure, rapid metabolism, and near-complete elimination of 14C metabolites in rats. Significance Statement Lipid 5 is a key component of lipid nanoparticles used for the delivery of mRNA-based medicines; understanding the rates and routes of its clearance is crucial to assessing its long-term safety in LNP technology. This study conclusively established the rapid metabolism, and near- complete elimination of intravenously administered [14C]Lipid 5 in rats via both liver and kidney as oxidative metabolites derived from ester hydrolysis and subsequent β-oxidation.

An Overview of Second Generation Nanoparticles− Nanostructure Lipid Carrier Drug Delivery System

Lipids are used as vehicles for the preparation of various formulations prescribed for administrations, including emulsions, ointments, suspension, tablets, and suppositories. The first parental nano-emulsion was discovered from the 1950s when it was added to the intravenous administration of lipid and lipid-soluble substances. Lipid-based drug delivery systems are important nowadays. Solid nanoparticles (SLN) and Nanostructured lipid carriers (NLC) are very proficient due to the ease of production process, scale-up capability, bio-compatibility, the biodegradability of formulation components and other specific features of the proposed route. The administration or nature of the materials must be loaded into these delivery systems. The main objectives of this review are to discuss an overview of second-generation nanoparticles, their limitations, structures, and route of administration, with emphasis on the effectiveness of such formulations. NLC is the second generation of lipid nanoparticles having a structure like nanoemulsion. The first generation of nanoparticles was SLN. The difference between both of them is at its core. Both of them are a colloidal carrier in submicron size in the range of 40-1000 nm. NLC is the most promising novel drug delivery system over the SLN due to solving the problem of drug loading and drug crystallinity. Solid and liquid lipids combination in NLC formation, improve its quality as compare to SLN. NLC has three types of structures: random, amorphous, and multiple. The random structure containing solid-liquid lipids and consisting crystal and the liquid lipid irregular in shape; thereby enhance the ability of the lipid layer to pass through the membrane. The second is the amorphous structure. It is less crystalline in nature and can prevent the leakage of the loaded drug. The third type is multiple structures, which have higher liquid lipid concentrations than other types. The excipients used to form the NLC are bio-compatible, biodegradable and non-irritating, most of which can be detected using GRAS. NLC is a promising delivery system to deliver the drug through pulmonary, ocular, CNS, and oral route of administration. Various methods of preparation and composition of NLC influence its stability Parameters. In recent years at the educational level, the potential of NLC as a delivery mechanism targeting various organs has been investigated in detail.

PT10.1: The Efficacy and Safety of High Dose Intravenous Lipid Administration to Extremely Low Birth Weight Infants in the Early Neonatal Period

PT10.1: The Efficacy and Safety of High Dose Intravenous Lipid Administration to Extremely Low Birth Weight Infants in the Early Neonatal Period

Differential Effects of Oral and Intravenous Lipid Administration on Key Molecules Related to Energy Homeostasis.

The spectrum of lipid-induced changes in the secretion of hormones important in energy homeostasis has not yet been fully elucidated. To identify potential incretin-like effects in response to lipid administration, we examined the short-term effect of iv vs oral lipids on key molecules regulating energy homeostasis. Design, Intervention, and Participants: After a 10-hour overnight fast, 26 subjects were randomized to receive an oral lipid load, a 10% iv lipid emulsion, a 20% iv lipid emulsion, or an iv saline infusion. We obtained blood samples at 30-minute intervals for the first 2 hours and hourly thereafter for a total of 6 hours. Circulating levels of insulin, glucose, c-peptide, free fatty acids, incretins (glucagon-like peptide-1, gastric inhibitory polypeptide), glucagon, peptide YY, ghrelin, fibroblast growth factor 21, fetuin A, irisin, omentin, and adiponectin were measured. Oral lipid ingestion resulted in higher glucagon-like peptide-1, gastric inhibitory polypeptide, glucagon, and peptide YY levels, compared with the other three groups (incremental area under the curve P = .003, P < .001, P < .001, P < .001, respectively). The 20% lipid emulsion, leading to higher free fatty acid levels, resulted in greater insulin, c-peptide, and fibroblast growth factor 21 responses compared with placebo and the other two groups (incremental area under the curve P = .002, P = .005, P < .001, P < .001, respectively). Omentin, adiponectin, fetuin A, and irisin levels were not affected by either mode of lipid administration. Metabolic responses to lipids depend on the route of administration. Only iv lipids trigger a dose-dependent fibroblast growth factor 21 secretion, which is nonglucagon mediated. Intravenous lipids also induce hyperinsulinemia without concurrent decreases in glucose, a phenomenon observed in insulin-resistant states. Orally administered lipids mostly affect gastrointestinal tract-secreted molecules important in glucose and energy homeostasis such as glucagon, incretins, and peptide YY.

Phytosterols, Lipid Administration, and Liver Disease During Parenteral Nutrition.

Phytosterols are plant-derived sterols that are structurally and functionally analogous to cholesterol in vertebrate animals. Phytosterols are found in many foods and are part of the normal human diet. However, absorption of phytosterols from the diet is minimal. Most lipid emulsions used for parenteral nutrition are based on vegetable oils. As a result, phytosterol administration occurs during intravenous administration of lipid. Levels of phytosterols in the blood and tissues may reach high levels during parenteral lipid administration and may be toxic to cells. Phytosterols are not fully metabolized by the human body and must be excreted through the hepatobiliary system. Accumulating scientific evidence suggests that administration of high doses of intravenous lipids that are high in phytosterols contributes to the development of parenteral nutrition-associated liver disease. In this review, mechanisms by which lipids and phytosterols may cause cholestasis are discussed. Human studies of the association of phytosterols with liver disease are reviewed. In addition, clinical studies of lipid/phytosterol reduction for reversing and/or preventing parenteral nutrition associated liver disease are discussed.

A Metabolomic Analysis of Two Intravenous Lipid Emulsions in a Murine Model

BackgroundParenteral nutrition (PN), including intravenous lipid administration, is a life-saving therapy but can be complicated by cholestasis and liver disease. The administration of intravenous soy bean oil (SO) has been associated with the development of liver disease, while the administration of intravenous fish oil (FO) has been associated with the resolution of liver disease. The biochemical mechanism of this differential effect is unclear. This study compares SO and FO lipid emulsions in a murine model of hepatic steatosis, one of the first hits in PN-associated liver disease.MethodsWe established a murine model of hepatic steatosis in which liver injury is induced by orally feeding mice a PN solution. C57BL/6J mice were randomized to receive PN alone (a high carbohydrate diet (HCD)), PN plus intravenous FO (Omegaven®; Fresenius Kabi AG, Bad Homburg VDH, Germany), PN plus intravenous SO (Intralipid®; Fresenius Kabi AG, Bad Homburg v.d.H., Germany, for Baxter Healthcare, Deerfield, IL), or a chow diet. After 19 days, liver tissue was harvested from all animals and subjected to metabolomic profiling.ResultsThe administration of an oral HCD without lipid induced profound hepatic steatosis. SO was associated with macro- and microvesicular hepatic steatosis, while FO largely prevented the development of steatosis. 321 detectable compounds were identified in the metabolomic analysis. HCD induced de novo fatty acid synthesis and oxidative stress. Both FO and SO relieved some of the metabolic shift towards de novo lipogenesis, but FO offered additional advantages in terms of lipid peroxidation and the generation of inflammatory precursors.ConclusionsImproved lipid metabolism combined with reduced oxidative stress may explain the protective effect offered by intravenous FO in vivo.

Lipid infusion in the management of poisoning: a report of 6 canine cases

Intravenous administration of lipid is a relatively new treatment in the management of toxicity from lipophilic compounds. It is used in human medicine in the treatment of toxicity from lipophilic...

Lipid infusion in the management of poisoning: a report of 6 canine cases

Intravenous administration of lipid is a relatively new treatment in the management of toxicity from lipophilic compounds. It is used in human medicine in the treatment of toxicity from lipophilic...

Intravenous lipid administration for drug-induced toxicity: a critical review of the existing data

Following the discovery that administration of intravenous lipid emulsion (ILE) may reverse the cardiac and neurological toxicity of certain local anesthetic agents, ILE’s potential role has recently been explored in the setting of toxicity attributed to a variety of different drugs. The potential mechanisms, safety and efficacy of this approach are considered in this review. Data are reviewed from 76 published reports involving ILE administration for severe drug toxicity, including 55 where toxicity was due to nonanesthetic agents. ILE was reported to exert a positive therapeutic effect in only a proportion of the reported cases, with greatest evidence of efficacy concerning local anesthetic agents. Administration has typically involved bolus administration followed by continuous maintenance infusion, and a number of different mechanisms are proposed, from preferential partitioning of the drug from cardiac tissue to the circulating lipid fraction and direct inotropic effects related to carnitine pathways and fatty acid oxidative metabolism. No major adverse effects have been encountered, but too few data exist to adequately address the safety profile of ILE.

Successful treatment of permethrin toxicosis in two cats with an intravenous lipid administration

The present work describes successful treatment of permethrin toxicosis in two cats with a novel therapy of intravenous lipid administration. Two cats presented in lateral recumbency and with generalized tremor after they had been incidentally treated with permethrin for flea control by their owners. Initial therapy consisted of diazepam, propofol, bathing, and intravenous fluids. After an initial bolus of 2mg/kg BW pentobarbital a pentobarbital continuous rate infusion (CRI) was started. Both cats received an emulsion of 20% soybean oil and 80% olive oil, commonly used as fat component of total parenteral nutrition in humans, later in the course of therapy. A bolus of 2 ml/kg BW of the emulsion followed by a CRI of 4 ml/kg BW/h for 4 hours was administered via a jugular catheter as reported previously. One cat received two cycles of therapy with intravenous lipid whereas the other cat needed just one application. Both cats recovered completely without requiring any further treatment. In conclusion, administration of intravenous lipids for permethrin toxicosis in cats is a novel treatment approach which seems to be highly effective in shortening the recovery time for permethrin toxicosis and possibly other fat-soluble toxins.

Lipid Emulsion as Rescue Therapy in Lamotrigine Overdose

Background Lamotrigine is a sodium channel blocking agent that is widely prescribed for treatment of seizure. Although life-threatening effects are rarely observed in overdose, some previous reports have described the occurrence of cardiac toxicity. The management of sodium channel blocking agent-induced cardiotoxicity conventionally requires sodium bicarbonate administration. Recent case reports describe intravenous lipid administration as a successful treatment for refractory cardiovascular collapse induced by sodium channel blocking medications. Objective The objective of this study is to report the use of intravenous lipid emulsion as adjunctive therapy in a case of lamotrigine overdose in which electrocardiographic changes were unresponsive to bicarbonate therapy. Case Report We report a case of intentional lamotrigine overdose in a 50-year-old woman who lost consciousness and developed electrocardiographic aberrations, including widening of QRS with occurrence of left bundle branch block. The patient was initially treated with sodium bicarbonate without effect. Recovery of cardiac conduction was rapidly achieved after infusion of a 20% lipid emulsion. The exact mechanism of action of lipid emulsion is not fully understood. The lipophilic properties of lamotrigine suggest that it was partially removed by the plasmatic lipid emulsion. Conclusion This case provides additional insight into the potential benefit of using lipid emulsion in refractory sodium channel blocking intoxications.

Preconditioning of latissimus dorsi muscle flaps with monophosphoryl lipid a.

The use of dynamic myoplasty to restore function to failing organs is an exciting new application of skeletal muscle flaps. A complication of large flap elevation that can compromise flap function is ischemia-induced necrosis; one approach to minimizing this is to pretreat tissues with ischemic preconditioning. The purpose of this study was to determine whether systemic administration of monophosphoryl lipid A, a drug known to mimic late-phase ischemic preconditioning in the heart, could reduce ischemia-induced necrosis in latissimus dorsi muscle flaps. Forty latissimus dorsi muscle flaps from 20 Sprague-Dawley rats were allocated into four groups. In group I (n = 10), flaps were not preconditioned and served as controls. In group II (n = 10), flaps received ischemic preconditioning with two 30-minute periods of ischemia interspersed by 10 minutes of reperfusion. In group III (n = 10), rats received an intravenous bolus of approximately 0.3 ml of monophosphoryl lipid A vehicle only. In group IV (n = 10), rats received an intravenous bolus of 450 microg/kg of monophosphoryl lipid A and vehicle. Twenty-four hours after treatment, all latissimus dorsi muscle flaps were elevated on a single neurovascular pedicle and subjected to 4 hours of ischemia. After 72 hours of reperfusion, latissimus dorsi muscles were harvested, weighed, stained with nitroblue tetrazolium, and assessed for percent necrosis using digitized images of muscle sections and computerized planimetry. The percent necrosis in ischemic preconditioning-treated flaps (group II) was significantly reduced by 57 percent (p < 0.05) compared with control flaps (group I). The percent necrosis in flaps treated with monophosphoryl lipid A (group IV) was significantly reduced by 58 percent (p < 0.05) compared with vehicle-control flaps (group III). There was no difference in mean percent necrosis between ischemic preconditioning (group II) and monophosphoryl lipid A-treated (group IV) flaps or between ischemic preconditioning-control (group I) and monophosphoryl lipid A vehicle-control (group III) flaps. Intravenous administration of systemic monophosphoryl lipid A mimics the late-phase protective effect of ischemic preconditioning in the authors' rat latissimus dorsi muscle flap model.

Lipids in Parenteral Nutrition

After completing this article, readers should be able to: 1. Identify clinical indicators for the use of medium-chain triglycerides as an enteral lipid source. 2. Describe appropriate infusion rates, rates of advancement, and methods of monitoring tolerance of intravenous lipids. ### Composition and Metabolism Early initiation of intravenous lipid administration is important because it increases energy intake through a small volume of parenteral fluid with low osmolality, provides essential fatty acids, and reduces carbon dioxide production relative to glucose as an energy substrate. The most widely available intravenous lipids are prepared from soybean oil or a combination of soybean and safflower oil. All of the emulsions are emulsified with egg yolk phospholipid, with glycerol added to achieve an isotonic solution (Table 1⇓). Emulsions containing mixtures of olive and soybean oil and medium-chain triglycerides (MCTs) and soybean oil are also available. Infusion of intravenous lipid and parenteral nutrition in the same line may protect against phlebitis and loss of the intravenous vein, possibly due to physical coating of the vein with the lipid particles or the reduced osmolality of the infused solutions. The osmolality of intravenous lipid solutions, irrespective of the lipid concentration, is 268 mOsm/L, making them safe for both central and peripheral lines. View this table: Table 1. Composition of Intravenous Lipids The intravenous lipid particles have similar diameters to chylomicrons and acquire apo C11 from native lipoproteins after infusion. Clearance of intravenous lipid triglycerides proceeds by lipoprotein lipase, as described in Figure 1. However, dyslipoproteinemia, characterized by elevation of serum cholesterol and phospholipid secondary to infusion of 10% intravenous lipid emulsions, is well-known. This can occur even in the absence of elevated serum triglycerides and is largely the result of accumulation of abnormal particles containing phospholipid and cholesterol. These particles are generally known as lipoprotein (Lp) X. LpXs are formed from phospholipid present in the emulsion in excess …

Gene Delivery to the Rat Liver Using Cationic Lipid Emulsion/DNA Complex: Comparison between Intra-arterial, Intraportal and Intravenous Administration

ObjectiveTo compare the efficiency of intra-arterial, intraportal, and intravenous administration of cationic lipid emulsion/DNA complex, as used for gene transfer to rat liver.Materials and MethodsDNA-carrier complex for the in-vivo experiment was prepared by mixing DNA and a cationic lipid emulsion. According to the administration route used (intra-arterial, intraportal, or intravenous), the animals were assigned to one of three groups. The heart, lung, liver, spleen and kidneys were removed and assayed for total protein and luciferase concentration.ResultsThe cationic lipid emulsion/DNA complex used successfully transfected the various organs via the different administration routes employed. Luciferase activity in each organ of untreated animals was negligible. Liver luciferase values were significantly higher in the groups in which intra-arterial or intraportal administration was used.ConclusionThe intra-arterial or intraportal administration of cationic lipid emulsion/DNA complex is superior to intravenous administration and allows selective gene transfer to the liver.

Role of nitric oxide in gastric relaxation induced by intravenous administration of lipid in conscious dogs

Role of nitric oxide in gastric relaxation induced by intravenous administration of lipid in conscious dogs

Optimization of Cationic Lipid/DNA Complexes for Systemic Gene Transfer to Tumor Lesions

Intravenous (i.v.) administration of cationic lipid N-[(l-(2-3-dioleyloxy)propyl)]-N-N-N-trimethylammonium chloride (DOTMA)-based transfection complexes in mice with subcutaneous squamous cell tumors yielded plasmid delivery and expression in tumor lesions. The efficiency of gene transfer in tumors was significantly lower than in the lung. This was consistent with low plasmid levels associated with the tumor, suggesting that plasmid delivery to the tumor site was a limiting factor. Lowering the lipid/DNA charge ratio from 5:1 to 0.8:1 (+/-) did not change DNA levels in tumor but significantly reduced DNA levels in lung. However, expression levels were significantly reduced in both tissues at lower lipid/DNA charge ratios. Complexes prepared from small unilamellar liposomes gave significantly lower expression levels in the lungs but similar expression levels in tumors when compared to complexes prepared from larger unilamellar liposomes. The small liposome complexes were better tolerated than large liposome complexes. Varying the cationic lipid to colipid (cholesterol or DOPE) molar ratio from 4:1 to 1:1 significantly reduced expression levels in both tumor and lung. Cationic lipid substitution, using a cholesterol cationic lipid, diethyldiamino-carbamyl-cholesterol instead of DOTMA, produced reduced expression in all other tissues except tumor. Incorporation of PEG into preformed transfection complexes reduced DNA delivery to lung, increased circulation half-life, and enhanced DNA delivery to tumor. In a lung metastatic mouse tumor model, where the accessibility of the i.v. administered transfection complexes to tumor lesions should be less challenging, DOTMA: CHOL complexes (4:1 lipid to colipid molar ratio, 3:1 ± lipid to plasmid charge ratio) were preferentially localized in tumor lesions. These data demonstrate that systemic gene transfer to distal tumor sites by lipid/DNA complexes may be limited by low plasmid delivery. Modifying the chemical surface properties of transfection complexes enhanced both DNA delivery and expression in tumor and is one approach that may overcome limitations.

In vivo gene transfer via intravenous administration of cationic lipid-protamine-DNA (LPD) complexes.

A novel LPD formulation has been developed for in vivo gene transfer. It involves the interaction of plasmid DNA with protamine sulfate, a cationic polypeptide, followed by the addition of DOTAP cationic liposomes. Compared with DOTAP/DNA complexes, LPD offers better protection of plasmid DNA against enzymatic digestion and gives consistently higher gene expression in mice via tail vein injection. When a luciferase reporter gene was employed, gene expression was found in all tissues examined including lung, heart, spleen, liver and kidney with the highest expression in the lung. The in vivo efficiency of LPD was dependent upon charge ratio and was also affected by the lipid used. Increasing the amount of DNA delivered induced an increase in gene expression. The optimal dose was approximately 50 micrograms per mouse at which concentration approximately 20 ng luciferase protein per milligram extracted tissue protein could be detected in the lung. Increasing the DNA to 100 micrograms per mouse resulted in toxicity and death of the animal. Gene expression in the lung was detected as early as 1 h after injection, peaked at 6 h and declined thereafter. High expression was also found in the spleen 6 h after injection but dropped very rapidly thereafter. The in vivo gene expression by LPD was dependent upon the route of administration since intraportal injection of LPD led to about a 100-fold decrease in gene expression in the lung as compared with i.v. injection. Using lacZ as a reporter gene, it was shown that endothelial cells were the primary locus of transgene expression in both the lung and spleen. No sign of inflammation in these organs was noticed. Since protamine sulfate has been proven to be nontoxic and only weakly immunogenic in humans, this novel vector may be useful for clinical gene therapy.

Effect of l-glutamine supplementation on impaired glucose regulation during intravenous lipid administration

In contrast to l-glutamine, lipid emulsions are routinely administered to patients receving nutritional support. The provision of fat during intravenous feeding is essential, but the potentially toxic byproducts of fatty acid oxidation may have adverse metabolic consequences. In the present study, we have examined the effect of l-glutamine, an inhibitor of fatty acid oxidation, on the development of defective blood glucose regulation caused by a 48-hour infusion of 10% intralipid in rats. Male Sprague-Dawley rats (200–290g) were anesthetized with sodium pentobarbital, the right femoral vein cannulated, and baseline blood samples were taken. Each rat was placed in a metabolic cage with access to water, in the presence or absence of rodent chow. Two hours after waking, the rats were infused with 10% intralipid with either saline (control), 2% l-glutamine, or 2% l-alanine. After 48 hours, all animals were sacrificed and blood samples were again obtained. The mean ± SEM plasma glucose levels before and after lipid infusion at the rate of 1 mL/hr in control rats fed ad libitum, were 125 ± 13 and 170 ± 5 mg/dL ( p < 0.01, n = 7). Similarly, plasma free fatty acids (FFA) in these animals rose from 0.74 ± 0.11 to 1.34 ± 0.32 mmol/L ( p < 0.05). Plasma insulin levels also increased from 337 ± 44 to 1278 ± 88 pg/mL ( p < 0.01). Reduction of intralipid dose infusion did not prevent insulin resistance characterized by hyperglycemia and hyperinsulinemia. However, addition of l-glutamine to the high-dose lipid infusion with chow feeding prevented changes in plasma glucose, insulin levels, and FFA but not triglyceride levels. Also, glutamine but not alanine supplementation in intralipid infused rats without chow feeding prevented changes in plasma glucose, insulin, and malondialdehyde levels. In conclusion, these data show that glutamine supplementation during intravenous lipid administration in rats prevents the development of impaired glucose regulation associated with hyperlipidemia.

Effect of ?-Glutamine Supplementation on Impaired Glucose Regulation During Intravenous Lipid Administration

Effect of ?-Glutamine Supplementation on Impaired Glucose Regulation During Intravenous Lipid Administration